The main objective of this research is to determine if estrogen regulated cytodifferentiation and glycoprotein biosynthesis in mammalian endocervical epithelia by the established estrogen-receptor mechanism. In order to define the regulator role of estrogen it is necessary to determine to what extent, if any, cellular differentiation precedes cellular competence to synthesize glycoproteins. We have previously established the estrogen-treated ovariectomized rabbit as a useful animal model in which to characterize early cytodifferentiative events. These events will be evaluated both ultrastructurally and histochemically. With this model it is then possible to determine if estrogen induces de novo glycoprotein biosynthesis or alternatively, if estrogen regulates glycosylation, i.e., co- and post-translational modifications of the molecule. The quanitative correlation of changes in glycoprotein biosynthetic activity with changes in progesterone receptor concentrations will serve as markers of estrogen-action. Specific glycoproteins will be identified and used to study the interaction of progesterone in the regulation of protein synthesis. Using a unit gravity cell separation procedure it will be possible to determine if specific epithelial cell types synthesize different glycoproteins. Finally, it will be possible to determine if changes in the hormonal milieu which are known to alter the cell populations also produce measurable changes in he glycoproteins they synthesize.